Inflammation augments the development of experimental glomerulonephritis by accelerating proteinuria and enhancing mortality

Proteinuria represents a parameter for a damaged filtration capacity of the kidney. We investigated how inflammation influences the development of experimental, immune complex-mediated glomerulonephritis by monitoring proteinuria. Mice pre-treated with LPS or TNF, one day before induction of glomerulonephritis, excreted high levels of protein in the urine immediately after the induction of glomerulonephritis, in contrast to non-treated mice where proteinuria increased steadily after day 3. Protein levels in the urine of pre-treated mice remained elevated over the 15-day observation time. The severity of proteinuria at later times correlated with the degree of tissue pathology and mortality in individual mice. Pre-treatment with inflammatory agents accelerated the development of proteinuria and induced more severe kidney damage.